Superoxide anion production in papillary muscle of SHAM, Ovariectomized (OVX), Ovariectomized plus carvedilol (OVX+CAR) at 60 days postsurgery.

<p>The values are expressed as the means ± S.E.M. * Significantly different from SHAM and # from OVX (<i>p</i><0.05) using one-way ANOVA and Tukey post hoc test.</p

Left ventricular collagen content.

<p>The data is expressed as the mean ± S.E.M. * <i>p</i><0.05 vs. SHAM rats. # <i>p</i><0.05 vs. OVX rats using one-way ANOVA and Tukey post hoc test. Number of animals in indicated in parenthesis.</p

Ponderal data from SHAM, Ovariectomized and Ovariectomized plus Carvedilol: BW, body weight (n = 7–9); LV/BW, left ventricle body weight ratio (n = 9–10); Uterus/BW, uterus body weight ratio (n = 8–10); Tibia length (n = 7–10); LV/Tibia, left ventricle tibia ratio (n = 14–19) and papillary muscle weight (n = 7–9).

<p>Data are shown as mean ± SEM.</p>*<p>p<0.05 versus Sham and #p<0.05 versus OVX.</p><p>ANOVA one way and Tukey test.</p

Glucose-6-Phosphate Dehydrogenase Deficiency Increases Myocardial Redox Stress and Moderately Accelerates the Development of Heart Failure

Background- Glucose 6-phosphate dehydrogenase (G6PD) is the most common deficient enzyme in the world. In failing hearts, G6PD is upregulated and generates reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is used by the glutathione pathway to remove reactive oxygen species but also as a substrate by reactive oxygen species-generating enzymes. Therefore, G6PD deficiency might prevent heart failure by decreasing NADPH and reactive oxygen species production. Methods and Results- This hypothesis was evaluated in a mouse model of human G6PD deficiency (G6PDX mice, ≈40% normal activity). Myocardial infarction with 3 months follow-up resulted in left ventricular dilation and dysfunction in both wild-type and G6PDX mice but significantly greater end diastolic volume and wall thinning in G6PDX mice. Similarly, pressure overload induced by transverse aortic constriction (TAC) for 6 weeks caused greater left ventricular dilation in G6PDX mice than wild-type mice. We further stressed transverse aortic constriction mice by feeding a high fructose diet to increase flux through G6PD and reactive oxygen species production and again observed worse left ventricular remodeling and a lower ejection fraction in G6PDX than wild-type mice. Tissue content of lipid peroxidation products was increased in G6PDX mice in response to infarction and aconitase activity was decreased with transverse aortic constriction, suggesting that G6PD deficiency increases myocardial oxidative stress and subsequent damage. Conclusions- Contrary to our hypothesis, G6PD deficiency increased redox stress in response to infarction or pressure overload. However, we found only a modest acceleration of left ventricular remodeling, suggesting that, in individuals with G6PD deficiency and concurrent hypertension or myocardial infarction, the risk for developing heart failure is higher but limited by compensatory mechanisms

Comenta&#769;rios a uma sentenc&#807;a anunciada : o processo Lula

“Comentários a uma sentença: o Caso Lula” é talvez o mais importante documento jurídico publicado no Brasil em décadas. A presente coletânea de artigos nasceu de um movimento espontâneo e bastante significativo de juristas brasileiros e estrangeiros que examinaram cuidadosamente a sentença proferida no âmbito do processo que tramitou na 13ª Vara Federal de Curitiba, no caso que ficou conhecido na mídia como o do “tríplex do Guarujá”. <br>De la presentación de Geraldo Prad